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Updated: Mar 9, 2026
Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization
Published on: March 2, 2017
Evaluation of deoxynivalenol-induced toxic effects on mouse endometrial stromal cells: Cell apoptosis and cell cycle
Yujian Dai1, Haiqiang Xie1, Yinxue Xu1
1College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Abstract:
Deoxynivalenol (DON) is a type B trichothecene mycotoxin which has toxic effects on humans and animals. Although DON has been studied in various cell types for its cytotoxicity, there is litter information about the effects of DON on mouse endometrial stromal cells (ESCs). Thus, in this study, we investigated the toxic effects of DON on mouse ESCs and its possible mechanisms. DON inhibited the cell viability in a dose- and time-dependent manner. TUNEL assay results showed that DON caused apoptosis and TUNEL-positive cells increased with increasing DON concentrations in mouse ESCs. Western blot showed that DON significantly increased the expression levels of apoptosis-related protein including Caspase-9, Caspase-3, poly (ADP-ribose) polymerase (PARP) and the ratio of Bax/Bcl-2. After DON treatment, the expression levels of cell cycle-related protein including p38/p-p38, Cdc25C/p-Cdc25C, Cdc2/p-Cdc2 and cyclinB1 were significantly decreased and immunoprecipitation analysis showed that cyclinB1-Cdc2 complex was significantly decreased. However, the combination of SB203580 (p38 specific inhibitor) and DON treatment significantly reversed the depression of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, cyclinB1 and cyclinB1-Cdc2 complex. Collectively, these data suggest that DON causes apoptosis via mitochondria apoptosis pathway and induces G2 arrest via p38 MAPK signaling pathway in mouse ESCs.
Insights
Deoxynivalenol (DON) causes cell death and cell cycle arrest in mouse endometrial stromal cells (ESCs). This mycotoxin induces apoptosis via the mitochondrial pathway and G2 arrest through the p38 MAPK signaling pathway.
Area of Science:
- Toxicology
- Cell Biology
- Molecular Biology
Background:
- Deoxynivalenol (DON) is a prevalent trichothecene mycotoxin with known toxic effects.
- Limited research exists on DON's impact on mouse endometrial stromal cells (ESCs).
Purpose of the Study:
- To investigate the toxic effects of DON on mouse ESCs.
- To elucidate the underlying mechanisms of DON-induced toxicity in these cells.
Main Methods:
- Cell viability assays were performed.
- Apoptosis was assessed using TUNEL assay.
- Protein expression levels (apoptosis and cell cycle markers) were analyzed via Western blot.
- Immunoprecipitation identified protein complex formation.
- p38 MAPK pathway involvement was confirmed using a specific inhibitor (SB203580).
Main Results:
- DON inhibited cell viability in a dose- and time-dependent manner.
- DON induced apoptosis and increased the Bax/Bcl-2 ratio.
- DON treatment led to G2 cell cycle arrest by downregulating key cell cycle proteins and the cyclinB1-Cdc2 complex.
- The p38 MAPK signaling pathway was identified as crucial for DON-induced G2 arrest.
Conclusions:
- DON induces apoptosis in mouse ESCs through the mitochondrial pathway.
- DON causes G2 cell cycle arrest in mouse ESCs mediated by the p38 MAPK signaling pathway.
